Relevant bibliographies by topics / Akt

Academic literature on the topic 'Akt'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Akt"

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Matheny, Ronald W., and Martin L. Adamo. "Current Perspectives on Akt Akt-ivation and Akt-ions." Experimental Biology and Medicine 234, no. 11 (November 2009): 1264–70. http://dx.doi.org/10.3181/0904-mr-138.

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Gömöri, George, and Piroska Szántó. "Akt." World Literature Today 70, no. 1 (1996): 212. http://dx.doi.org/10.2307/40151976.

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Kotecha, Anish. "AKT question relating to Mental Health Act." InnovAiT: Education and inspiration for general practice 10, no. 11 (October 13, 2017): e139-e139. http://dx.doi.org/10.1177/1755738017728167.

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Abdel Kerim, Yasser. "AKT question relating to Mental Health Act." InnovAiT: Education and inspiration for general practice 10, no. 11 (October 13, 2017): e147-e147. http://dx.doi.org/10.1177/1755738017728180.

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Dunn, Ewan F., Rachel Fearns, and John H. Connor. "Akt Inhibitor Akt-IV Blocks Virus Replication through an Akt-Independent Mechanism." Journal of Virology 83, no. 22 (September 9, 2009): 11665–72. http://dx.doi.org/10.1128/jvi.01092-09.

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ABSTRACT Many viruses activate the phosphatidylinositol 3′-kinase (PI3k)/Akt intracellular signaling pathway to promote viral replication. We have analyzed whether a rapidly replicating rhabdovirus, vesicular stomatitis virus (VSV), requires the PI3k/Akt signaling pathway for its replication. Through the use of chemical inhibitors of PI3k and Akt, we show that VSV replication and cytopathic effects do not require activation of these kinases. Inhibitors that block the activating phosphorylations of Akt at threonine 308 (Thr308) and serine 473 (Ser473) did not inhibit VSV protein expression or the induction of the cytopathic effects of VSV. One compound, Akt inhibitor Akt-IV, inhibited the replication of VSV, respiratory syncytial virus, and vaccinia virus but increased the phosphorylation of Akt at positions Thr308 and Ser473 and did not inhibit Akt kinase activity in vitro. Together, our data suggest that the PI3k/Akt pathway is of limited relevance to the replication of VSV but that Akt inhibitor Akt-IV is a novel broad-spectrum antiviral compound with a mechanism differing from that of its previously reported effect on the PI3k/Akt pathway. Identification of other targets for this compound may define a new approach for blocking virus replication.
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Danwerth, Christopher. "Die virtuelle Hauptversammlung – Dritter Akt! Letzter Akt?" Die Aktiengesellschaft 66, no. 19 (October 1, 2021): r283—r284. http://dx.doi.org/10.9785/ag-2021-661903.

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Kumar, Chandra C., and Vincent Madison. "AKT crystal structure and AKT-specific inhibitors." Oncogene 24, no. 50 (November 2005): 7493–501. http://dx.doi.org/10.1038/sj.onc.1209087.

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Nandakumar, Michael. "AKT question relating to the Mental Capacity Act." InnovAiT: Education and inspiration for general practice 7, no. 12 (December 2014): 767. http://dx.doi.org/10.1177/1755738014557737.

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Abdel Kerim, Yasser. "AKT question relating to Mental Health Act assessments." InnovAiT: Education and inspiration for general practice 10, no. 11 (October 13, 2017): e145-e145. http://dx.doi.org/10.1177/1755738017728178.

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Nandakumar, M. "AKT question relating to Mental Health Act 2007." InnovAiT 4, no. 5 (May 1, 2011): 287. http://dx.doi.org/10.1093/innovait/inr077.

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Dissertations / Theses on the topic "Akt"

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Mahnel, Petr. "Optimalizace výroby firmy AKT." Master's thesis, Vysoká škola ekonomická v Praze, 2009. http://www.nusl.cz/ntk/nusl-72128.

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This thesis aims to provide a reader with practical example of optimization achieved using the Lingo software. The main focus is improvement of efficiency and shortening of a production process in AKT, a company engaged in production of car parts. It is a software, which accommodates needs of the company as well as production requirements. The theoretical part is focused on detailed description of methods and procedures used in a practical part. These methods should help the reader to understand a nature of formulas relevant for the subject. Practical part focuses on the optimization using data obtained from the company AKT, evaluation of the data and subsequent consultations with a manager of production, followed by the assessment of practical relevance for the production.
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Aiken, Andrew. "AKT-R4 a diagnosis tool." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25223.

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Meadows, Kafi, Seema Iyer, Mark Stevens, Duanning Wang, Sharon Shechter, Carole Perruzzi, Todd Camenisch, and Laura Benjamin. "Akt promotes Endocardial-Mesenchyme Transition." BioMed Central, 2009. http://hdl.handle.net/10150/610167.

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Endothelial to mesenchyme transition (EndMT) can be observed during the formation of endocardial cushions from the endocardium, the endothelial lining of the atrioventricular canal (AVC), of the developing heart at embryonic day 9.5 (E9.5). Many regulators of the process have been identified
however, the mechanisms driving the initial commitment decision of endothelial cells to EndMT have been difficult to separate from processes required for mesenchymal proliferation and migration. We have several lines of evidence that suggest a central role for Akt signaling in committing endothelial cells to enter EndMT. Akt1 mRNA was restricted to the endocardium of endocardial cushions while they were forming. The PI3K/Akt signaling pathway is necessary for mesenchyme outgrowth, as sprouting was inhibited in AVC explant cultures treated with the PI3K inhibitor LY294002. Furthermore, endothelial marker, VE-cadherin, was downregulated and mesenchyme markers, N-cadherin and Snail, were induced in response to expression of a constitutively active form of Akt1 (myrAkt1) in endothelial cells. Finally, we isolated the function of Akt1 signaling in the commitment to the transition using a transgenic model where myrAkt1 was pulsed only in endocardial cells and turned off after EndMT initiation. In this way, we determined that increased Akt signaling in the endocardium drives EndMT and discounted its other functions in cushion mesenchymal cells.
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Park, Sungman. "AKT function and human oncogenesis." [Tampa, Fla.] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001885.

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Palková, Anežka. "Spolupráce EU - AKT na příkladu Haiti." Master's thesis, Vysoká škola ekonomická v Praze, 2011. http://www.nusl.cz/ntk/nusl-113492.

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This thesis focuses on cooperation of the European Union with the African, Carribean and Pacific Group of States. Its aim is to describe the relations in a complex way and to record the changes that are connected with the evolution of cooperation. Attention is also paid to conditionality of cooperation. Introductory part describes EU development cooperation and humanitarian aid. Historical evolution of EU-ACP cooperation follows together with the details on the Cotonou Agreement. Last part is the case study on Haiti.
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Middel, Ines Kristin. "Quantitative Untersuchung der Proteinkinase AKT am Ovarialkarzinom." Köln Deutsche Zentralbibliothek für Medizin, 2010. http://d-nb.info/1000727416/34.

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Ng, Foong Loo Yvonne Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Insulin action: unravelling AKT signalling in Adipocytes." Awarded by:University of New South Wales. Biotechnology & Biomolecular Sciences, 2009. http://handle.unsw.edu.au/1959.4/44628.

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The Ser/Thr kinase Akt plays an important role in many of insulin's actions including GLUT4 translocation to the plasma membrane (PM). However, there are several features of Akt's regulation of GLUT4 translocation that remain unclear. The goal of my thesis was to resolve some of the following questions: Is activation of Akt sufficient to stimulate GLUT4 translocation? What is the quantitative relationship in signal transmission between individual components within the Akt cascade? What is the role of Akt in insulin resistance? To determine if activation of Akt is sufficient to mediate GLUT4 translocation, I developed a drug-inducible heterodimerisation strategy to activate Akt2 independently of other potential insulin signalling pathways. These studies revealed that activation of Akt2 resulted in rapid stimulation of GLUT4 translocation to a similar extent with maximum insulin, indicating that Akt2 is sufficient for this event. It was previously observed that maximum effect of insulin on GLUT4 translocation was obtained with minimum activation of Akt. To resolve this discrepancy, the relationship between Akt signalling components was examined using a quantitative kinetic and dose response approach combined with hierarchical cluster analysis. Most notably I observed a strong relationship between Akt at the PM, but not Akt in the whole cell lysate, with its substrate phosphorylation. Active pools of phospho-Akt and -AS160, a major substrate involved in GLUT4 translocation, were found in the lipid raft, highlighting the importance of subcellular partitioning of key signalling components for achieving biological specificity. The involvement of Akt in insulin resistance was investigated using the heterodimerisation strategy. These studies revealed that insulin itself initiates a pathway that causes insulin resistance by converging on target(s) downstream of Akt. This inhibitory pathway emanates from PI3-kinase and is likely induced by a range of insults including chronic insulin and dexamethasone. In conclusion, Akt is a crucial element in the insulin action pathway that exhibits precise spatial regulation. While the role of this nanoregulation of Akt in disease remains to be evaluated, my studies suggest that the major defect contributing to insulin resistance occurs downstream of Akt. The elucidation of this target will have major implications for metabolic diseases.
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Rickle, Annika. "PTEN and Akt signalling in Alzheimer's disease /." Stockholm : Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-514-3/.

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Hiester, Andreas [Verfasser]. "Proteininteraktion der Proteinkinase AKT 1 / Andreas Hiester." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2014. http://d-nb.info/1046174215/34.

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Fedrigo, Carlos Alexandre. "Inibição da via PI3K-Akt em gliomas." Pontifícia Universidade Católica do Rio Grande do Sul, 2012. http://hdl.handle.net/10923/4518.

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Glioblastoma multiforme (GMB) is the most malignant and common type of all astrocytic tumours. Current standard treatment for GBM patients involves maximum surgical resection of the tumour, followed by radiotherapy and chemotherapy, usually containing the alkylating agent Temozolomide (TMZ). Despite this aggressive combination therapy, the survival rate of GBM patients is still low. This work consisted in investigating the cytotoxic effects of Akt-inhibition by MK-2206 with irradiation (RT) and TMZ on in vitro human malignant glioma. Seven malignant glioma cell lines were cultured and tested for clonogenic survival, invasion inhibition, tumour spheroid growth and proliferation. The Akt-inhibitor MK-2206 and TMZ were added at different time treatments and in varying doses. Cultures were irradiated with single dose and with fractionated γ-irradiation. Cellular modulation of Akt and p-Akt were assessed by Western blot analysis. MK-2206 reduced the levels of phospho- Akt key protein in the PI3Kinase-Akt pathway, decreased cell survival, and inhibited invasion, proliferation and cell growth. The combination of MK-2206 and RT lead to enhanced inhibition of cell proliferation and invasion, which is not observed with RT alone. The radioenhancing effect of MK-2206 was most striking in inhibition of spheroid volume growth by fractionated RT; the radiosensitizing effect of MK-2206 was stronger than that of TMZ. MK-2206 enhanced the in vitro effects of RT and TMZ in terms of decreased cell survival, invasion, proliferation and growth in malignant glioma. Effects could be ascribed to inhibition of PI3K-Akt pathway.
O Glioblastoma multiforme (GBM) é o tipo mais maligno e mais comum de todos tumores astrocíticos. O tratamento atual para pacientes de GBM envolve máxima remoção cirúrgica, seguida de radio e quimioterapia, normalmente com o agente alquilante Temozolamida (TMZ). Apesar da agressividade da terapia combinada, o tempo de sobrevivência dos pacientes ainda é baixo. Este trabalho procurou investigar os efeitos citotóxicos do inibidor de Akt MK-2206 em combinação com irradiação (RT) e TMZ em um painel de células de gliomas humanos. Sete linhagens de glioma foram cultivadas e testadas em ensaio de sobrevivência clonogênica, inibição de invasão, e modelos de proliferação e crescimento de volume em esferóides. O inibidor MK-2206 e TMZ foram adicionados em diferentes tempos de tratamento e diferentes doses. As culturas foram irradiadas com doses únicas ou em terapias fracionadas com irradiação γ. A modulação celular de Akt e fosfo-Akt foi checada via Western Blot. O composto MK-2206 reduziu a fosforilação da proteína chave Akt na via PI3K, diminuindo a sobrevivência celular e inibindo invasão, proliferação e crescimento celular. A combinação de MK-2206 com RT levou a uma maior inibição de invasão e proliferação, o que não é observado somente com a RT. O efeito radiosensível de MK-2206 foi ainda maior na inibição do volume dos esferóides em terapia combinada com RT fracionada, sendo ainda maior do que o efeito combinado com TMZ. MK-2206 aumentou os efeitos in vitro de RT e TMZ em termos de redução de sobrevivência celular, invasão, proliferação e crescimento celular em gliomas malignos. Os efeitos podem ser atribuídos a inibição da via PI3KAkt.
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Books on the topic "Akt"

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Szántó, Piroska. Akt. Budapest: Európa, 1994.

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Fösterling, Hermann. Akt. Frankfurt Main: Umschau/Braus, 2000.

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Dugalić, Ljiljana. Akt. 2nd ed. Beograd: Ljiljana Dugalić, 2008.

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1936-, Dabo Radoslav, and Čegec Branko, eds. Akt. Zagreb: Meandar, 1999.

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Dugalić, Ljiljana. Akt. 2nd ed. Beograd: Ljiljana Dugalić, 2008.

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Jutarnyj akt. Beograd: Čigoja štampa, 2000.

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Krolikowski, Bohdan. Akt oskarzenia. Lublin: Wydawnictwo Katolickiego Uniwersytetu Lubelskiego, 2007.

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Akt oskarżenia. Lublin: Wydawnictwo KUL, 2007.

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Stalev, Zhivko Stoi︠a︡nov. Notarialnii︠a︡t akt. 2nd ed. Sofii︠a︡: Izdatelstvo za pravna literatura "Fenei︠a︡", 2004.

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Janssen, Sammlung. Manner Akt. Berlin: Janssen Verlag, 1992.

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Book chapters on the topic "Akt"

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Blaustein, Matías. "AKT." In Encyclopedia of Signaling Molecules, 267–80. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101974.

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Yap, Timothy A., and Johann S. de Bono. "AKT." In Cancer Therapeutic Targets, 3–12. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_35.

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Blaustein, Matías. "AKT." In Encyclopedia of Signaling Molecules, 1–14. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101974-1.

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Yap, Timothy A., and Johann S. de Bono. "AKT." In Cancer Therapeutic Targets, 1–10. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_35-5.

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Lœffler, Peter. "Akt I." In Guillaume Apollinaire die Brueste des Tiresias, 22–48. Basel: Birkhäuser Basel, 1989. http://dx.doi.org/10.1007/978-3-0348-6636-1_4.

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Lœffler, Peter. "Akt II." In Guillaume Apollinaire die Brueste des Tiresias, 49–75. Basel: Birkhäuser Basel, 1989. http://dx.doi.org/10.1007/978-3-0348-6636-1_5.

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Krebs, Anna-Maria, and Oliver Gollanek. "Dritter Akt." In Die Digitalisierung und der Faktor Mensch, 117–38. Wiesbaden: Springer Fachmedien Wiesbaden, 2019. http://dx.doi.org/10.1007/978-3-658-27992-9_6.

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Friedl, Christian. "Der erste Akt." In Hollywood im journalistischen Alltag, 1–120. Wiesbaden: Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16674-8_1.

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Friedl, Christian. "Der zweite Akt." In Hollywood im journalistischen Alltag, 121–232. Wiesbaden: Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16674-8_2.

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Friedl, Christian. "Der dritte Akt." In Hollywood im journalistischen Alltag, 233–89. Wiesbaden: Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16674-8_3.

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Conference papers on the topic "Akt"

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Nag, Arundhati. "Abstract 2172: Circle Akt in: Epitope catalyzed assembly of macrocyclic therapeutics against phosphorylated Akt." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2172.

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Berndt, Norbert, Hua Yang, Bernard Trinczek, Ziming Zhang, Bainan Wu, Nicholas J. Lawrence, Maurizio Pellechia, Ernst Schonbrunn, Jin Q. Cheng, and Said M. Sebti. "Abstract 3680: The Akt activation inhibitor TCN-P inhibits Akt phosphorylation by binding to the PH domain of Akt and blocking its recruitment to the plasma membrane." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3680.

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Ni, Qiang, Matthew Fosbrink, and Jin Zhang. "Illuminating the phosphatidylinositol 3-kinase/Akt pathway." In Biomedical Optics (BiOS) 2008, edited by Alexander P. Savitsky, Robert E. Campbell, and Robert M. Hoffman. SPIE, 2008. http://dx.doi.org/10.1117/12.765524.

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Ali, Amna, and Diane F. Matesic. "Abstract 4523: Chaetoglobosin K, a dual Akt and JNK inhibitor, modulates Akt phosphorylation in an mTORC2 independent manner." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4523.

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Ellington, Allison, Seamus Webb, Thomas Miller, Paula Eason, Leonid Dzantiev, Sripriya Ranganathan, Laura Schaefer, Pankaj Oberoi, and Jacob N. Wohlstadter. "Abstract 5159: Quantitative immunoassays to measure total Akt-1 and phospho-Akt(Ser473) in cell and tissue lysate models." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5159.

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Chebotariova, Nataliia Andreevna. "Arkhitektura kak akt kommunikatsii v rabotakh Umberto Eko." In IV International Research-to-practice conference. TSNS Interaktiv Plus, 2018. http://dx.doi.org/10.21661/r-469450.

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Li, Y., Y. Yang, Y. W. Wang, F. S. Shi, Y. Zhang, H. W. Wen, Q. Wang, J. Yang, L. Wang, and G. Yu. "TRIM36 Degrades Phosphorylated AKT to Suppress Pulmonary Fibrosis." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2466.

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Rajesh, SA, L. Coltan, A. Barr, JR Dyck, F. Eaton, and B. Thebaud. "Akt Activation Protects Lung Alveoli from Oxidant-Induced Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1970.

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Bryant, Latoya K., Kia J. Jones, and Cimona V. Hinton. "Abstract 501: CXCR4 induced ROS accumulation through PI3K/AKT." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-501.

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Spirina, L. V., Y. A. Usynin, I. V. Kondakova, Z. A. Yurmazov, E. M. Slonimskaya, and E. S. Kolegova. "The AKT-mTOR signalling pathway in kidney cancer tissues." In NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4936067.

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Reports on the topic "Akt"

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Baldwin, Albert S. Control of Akt Activity in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada512632.

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Chang, Chawnshang. Suppression of Androgen Receptor Transactivation by Akt Kinase. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada444244.

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Hager, Martin H. Membrane Heterogeneity in Akt Activation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada484355.

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Chung, Jun, and Arthur M. Mercurio. Integrin Regulation of Akt and Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada407289.

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Roper, Jatin. The Role of Akt Isoforms in Colorectal Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada613186.

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Hager, Martin H. Membrane Heterogeneity in Akt Activation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada538836.

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Hager, Martin H. Membrane Heterogeneity in Akt Activation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada504765.

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Hager, Martin H. Membrane Heterogeneity in Akt Activation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada510139.

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Chang, Chanshang. Suppression of Androgen Receptor Transactivation by Akt Kinase. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada423309.

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Shareef, Mohammed M., Biju Isaac, Sakhi Philip, Thirupandiyur Udayakumar, and Alan Pollack. AKT in Differential miRNA Processing in Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada593281.

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